Related Experiment Videos
Plasma levels of soluble CD30 are increased in children with chronic renal failure and with primary growth deficiency
G Barbano1, F Cappa, I Prigione
1Department of Pediatric Nephrology, Giannina Gaslini Institute, Children's Hospital, Largo G. Gaslini 5, I-16148 Genoa, Italy.
Insights
Growth hormone (GH) treatment reduced soluble CD30 (sCD30) levels in children with chronic renal failure (CRF) and GH deficiency. This suggests GH may influence the Th1/Th2 immune balance in these conditions.
Area of Science:
- Immunology
- Endocrinology
- Pediatrics
Background:
- Elevated soluble CD30 (sCD30) levels are linked to Th2 lymphocyte activation.
- Hormones like dehydroepiandrosterone, glucocorticoids, and progesterone modulate Th1/Th2 balance.
- Growth hormone (GH) is known to enhance lymphocyte function.
Purpose of the Study:
- To measure sCD30 plasma levels in children with growth failure due to chronic renal failure (CRF) or isolated GH deficiency.
- To evaluate the effect of recombinant human GH (rhGH) treatment on sCD30 levels and the Th1/Th2 balance.
Main Methods:
- sCD30 plasma levels were measured using ELISA in 30 children with CRF, 5 with isolated GH deficiency, and 10 controls.
- Measurements were taken before and after rhGH treatment in children with CRF and GH deficiency.
Main Results:
- Children with CRF had significantly higher sCD30 levels than controls, inversely correlated with glomerular filtration rate (GFR).
- rhGH treatment led to a significant decrease in sCD30 levels in children with CRF and those with primary GH deficiency.
- Children with primary GH deficiency also exhibited higher sCD30 levels compared to controls.
Conclusions:
- rhGH treatment reduced sCD30 plasma levels in children with CRF and GH deficiency.
- These findings suggest that GH may play a role in regulating CD30 expression and potentially the Th1/Th2 immune balance.
- Further research is needed to determine if the increase in sCD30 in uremia is due to reduced renal excretion, overproduction, or both.
Background:
Previous studies have suggested that in vivo Th2 lymphocyte activation is related to increased soluble CD30 (sCD30) plasma levels. As various hormones (dehydroepiandrosterone, glucocorticoids, progesterone) can regulate the Th1/Th2 balance, and because growth hormone (GH) enhances lymphocyte function, we measured sCD30 plasma levels, before and after treatment with recombinant human GH (rhGH), in children with growth failure due to chronic renal failure (CRF) or to isolated GH deficiency in order to evaluate the potential effects of rhGH treatment on Th1/Th2 balance.
Methods:
sCD30 plasma levels were determined by ELISA assay in 30 children with CRF (mean age 10.7+/-3.7 years), in five children with isolated GH deficiency (mean age 11.4+/-2.6 years), and in 10 normal controls (mean age 10.1+/-3.5 years).
Results:
sCD30 levels were higher in the 30 children with CRF than in the 10 controls (179.8+/-79.4 vs 11.3+/-10.9 U/ml, P<0.001) exhibiting an inverse correlation with glomerular filtration rate (GFR) (r=-0.7860, P<0.001). In 11 children with CRF, after 19.9+/-16.7 months of rhGH treatment, a decrease of sCD30 plasma level (170+/-50 vs 134+/-49 U/ml, P<0.01) was observed. The five children with primary GH deficiency had higher sCD30 plasma level than controls (mean 147+/-105 vs 11+/-10 U/ml, P<0.004) and sCD30 plasma levels decreased to 95.2+/-109.6 U/ml after rhGH treatment.
Conclusions:
The finding that rhGH treatment decreased sCD30 plasma levels in children with CRF, and that children with primary GH deficiency had higher sCD30 plasma levels than controls, suggest that GH may regulate CD30 expression and possibly the balance of Th1/Th2. Whether the uraemia-induced increase in sCD30 is due to decreased renal excretion, to overproduction or both, remains to be determined.